Anthropometric Measurements as Predictors of Low Birth Weight Among Tanzanian Neonates: A Hospital-Based Study
November 7, 2025
Background
The DSM defines panic attacks as an abrupt rush of severe fear or distress that peaks within minutes. Four or more specific physical symptoms characterize a panic attack.
Accelerated heart rate, sweating, trembling; sensations of suffocating; choking, chest pain, nausea, or abdominal distress; dizzy, unsteady, shivers, or warmth sensations and paresthesia.
Epidemiology
Compared to the general population, individuals with panic disorder have significantly greater lifelong rates of gastrointestinal, cardiovascular, pulmonary, and other health disorders. Panic disorder is more prevalent in European Americans than Latinos,
Asian Americans, or African Americans; Females are more susceptible than males. Panic disorder often observed more in adolescents and young adults, with individuals under 14 having a less incidence.
Patients share many additional comorbidities with panic disorders, such as social phobia, OCD, COPD, asthma, mitral valve prolapse, irritable bowel syndrome, and hypertension. Pregnant women with panic disorder are likelier to have infants with low birth weight.
Anatomy
Pathophysiology
Many peptides and neurotransmitters in the central nervous system influence physical manifestations significantly. Brain imaging examinations have revealed specific alterations, such as enhanced flow and receptor activation, in specific regions involving the frontal and limbic regions. The amygdala is thought to be the primary source of dysfunction.
Clinical illness and panic disorder are closely connected from a pathophysiological and psychological perspective. Two major hypotheses describe how patients are more susceptible to panic attacks. According to the first theory, susceptible individuals do not have the correct neurochemical mechanisms to control serotonin, so when it is high,
the model of the fear network in the autonomic nervous system is altered. According to the second hypothesis, a lack of endogenous opioids causes separation anxiety and an increased feeling of suffocation.
Etiology
Most theory points to a chemical imbalance as a primary contributor, such as irregularities in serotonin, cortisol, and gamma-aminobutyric acid. An environmental and genetic component is considered to have a role in the etiology of panic disorder. According to a few studies, stressful childhood events might lead to panic disorder among adults.
A newer study suggests neural circuitry plays a more significant part in panic disorder, where some brain sections are hyperexcitable in patients, predisposing them to the illness. According to specific research, genetic factors potentially contribute to the genesis of panic disorder.
First-degree relatives have a 40% likelihood of developing the syndrome if a family member has already been diagnosed. Individuals with panic disorder are also at a high risk of developing other mental health conditions.
Genetics
Prognostic Factors
The prognosis is questionable. It is unusual to have panic disorder without underlying disorders. Even after a symptom-free phase, most individuals will have a recurrence of symptoms.
Treatment adherence is a serious concern, and relapse of symptoms is prevalent. Only roughly 60% of patients reach remission in 6 months.
Chronic illnesses, high interpersonal sensitivity, marital status, belonging to low socioeconomic status, and living alone are all risk factors for poor outcomes. Such individuals are at risk for suicide and premature unfavorable cardiac events.
Clinical History
Physical Examination
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
by Stage
by Modality
Chemotherapy
Radiation Therapy
Surgical Interventions
Hormone Therapy
Immunotherapy
Hyperthermia
Photodynamic Therapy
Stem Cell Transplant
Targeted Therapy
Palliative Care
Medication
10
mg
Orally 
every day
and increase up to 10-40 mg/day orally
The Maximum dose for a day is 60 mg
0.25
mg
Tablet
Orally 
every 12 hrs
3
days
An immediate-release tablet of 0.5 mg is recommended orally every 8 hours for 4 days
An extended-release tablet of 0.5-1 mg orally each day. May increase the dose by 1 mg/day every 3-4 days
Average dose is 3-6 mg orally each day
An immediate-release tablet of 0.5 mg is recommended orally every 8 hours for 4 days
An extended-release tablet of 0.5-1 mg orally each day. May increase the dose by 1 mg/day every 3-4 days
Average dose is 3-6 mg orally each day
25 mg orally each day as a tablet
May increase the dose by 25 mg weekly
Do not exceed the dose of more than 200 mg each day
10 mg orally each day for the first week; later, 20 mg orally each day
Increase the dose gradually after several weeks
Do not exceed the dose of more than 60 mg each day
12
g
Orally 
once a day
1
month
(off-label):
50 mg/day orally at bedtime or 100 mg/day orally at bedtime as needed 
or 100-300 mg/day orally 
The maximum dose a day is 300 mg
Future Trends
References
https://www.ncbi.nlm.nih.gov/books/NBK430973/
The DSM defines panic attacks as an abrupt rush of severe fear or distress that peaks within minutes. Four or more specific physical symptoms characterize a panic attack.
Accelerated heart rate, sweating, trembling; sensations of suffocating; choking, chest pain, nausea, or abdominal distress; dizzy, unsteady, shivers, or warmth sensations and paresthesia.
Compared to the general population, individuals with panic disorder have significantly greater lifelong rates of gastrointestinal, cardiovascular, pulmonary, and other health disorders. Panic disorder is more prevalent in European Americans than Latinos,
Asian Americans, or African Americans; Females are more susceptible than males. Panic disorder often observed more in adolescents and young adults, with individuals under 14 having a less incidence.
Patients share many additional comorbidities with panic disorders, such as social phobia, OCD, COPD, asthma, mitral valve prolapse, irritable bowel syndrome, and hypertension. Pregnant women with panic disorder are likelier to have infants with low birth weight.
Many peptides and neurotransmitters in the central nervous system influence physical manifestations significantly. Brain imaging examinations have revealed specific alterations, such as enhanced flow and receptor activation, in specific regions involving the frontal and limbic regions. The amygdala is thought to be the primary source of dysfunction.
Clinical illness and panic disorder are closely connected from a pathophysiological and psychological perspective. Two major hypotheses describe how patients are more susceptible to panic attacks. According to the first theory, susceptible individuals do not have the correct neurochemical mechanisms to control serotonin, so when it is high,
the model of the fear network in the autonomic nervous system is altered. According to the second hypothesis, a lack of endogenous opioids causes separation anxiety and an increased feeling of suffocation.
Most theory points to a chemical imbalance as a primary contributor, such as irregularities in serotonin, cortisol, and gamma-aminobutyric acid. An environmental and genetic component is considered to have a role in the etiology of panic disorder. According to a few studies, stressful childhood events might lead to panic disorder among adults.
A newer study suggests neural circuitry plays a more significant part in panic disorder, where some brain sections are hyperexcitable in patients, predisposing them to the illness. According to specific research, genetic factors potentially contribute to the genesis of panic disorder.
First-degree relatives have a 40% likelihood of developing the syndrome if a family member has already been diagnosed. Individuals with panic disorder are also at a high risk of developing other mental health conditions.
The prognosis is questionable. It is unusual to have panic disorder without underlying disorders. Even after a symptom-free phase, most individuals will have a recurrence of symptoms.
Treatment adherence is a serious concern, and relapse of symptoms is prevalent. Only roughly 60% of patients reach remission in 6 months.
Chronic illnesses, high interpersonal sensitivity, marital status, belonging to low socioeconomic status, and living alone are all risk factors for poor outcomes. Such individuals are at risk for suicide and premature unfavorable cardiac events.
https://www.ncbi.nlm.nih.gov/books/NBK430973/
The DSM defines panic attacks as an abrupt rush of severe fear or distress that peaks within minutes. Four or more specific physical symptoms characterize a panic attack.
Accelerated heart rate, sweating, trembling; sensations of suffocating; choking, chest pain, nausea, or abdominal distress; dizzy, unsteady, shivers, or warmth sensations and paresthesia.
Compared to the general population, individuals with panic disorder have significantly greater lifelong rates of gastrointestinal, cardiovascular, pulmonary, and other health disorders. Panic disorder is more prevalent in European Americans than Latinos,
Asian Americans, or African Americans; Females are more susceptible than males. Panic disorder often observed more in adolescents and young adults, with individuals under 14 having a less incidence.
Patients share many additional comorbidities with panic disorders, such as social phobia, OCD, COPD, asthma, mitral valve prolapse, irritable bowel syndrome, and hypertension. Pregnant women with panic disorder are likelier to have infants with low birth weight.
Many peptides and neurotransmitters in the central nervous system influence physical manifestations significantly. Brain imaging examinations have revealed specific alterations, such as enhanced flow and receptor activation, in specific regions involving the frontal and limbic regions. The amygdala is thought to be the primary source of dysfunction.
Clinical illness and panic disorder are closely connected from a pathophysiological and psychological perspective. Two major hypotheses describe how patients are more susceptible to panic attacks. According to the first theory, susceptible individuals do not have the correct neurochemical mechanisms to control serotonin, so when it is high,
the model of the fear network in the autonomic nervous system is altered. According to the second hypothesis, a lack of endogenous opioids causes separation anxiety and an increased feeling of suffocation.
Most theory points to a chemical imbalance as a primary contributor, such as irregularities in serotonin, cortisol, and gamma-aminobutyric acid. An environmental and genetic component is considered to have a role in the etiology of panic disorder. According to a few studies, stressful childhood events might lead to panic disorder among adults.
A newer study suggests neural circuitry plays a more significant part in panic disorder, where some brain sections are hyperexcitable in patients, predisposing them to the illness. According to specific research, genetic factors potentially contribute to the genesis of panic disorder.
First-degree relatives have a 40% likelihood of developing the syndrome if a family member has already been diagnosed. Individuals with panic disorder are also at a high risk of developing other mental health conditions.
The prognosis is questionable. It is unusual to have panic disorder without underlying disorders. Even after a symptom-free phase, most individuals will have a recurrence of symptoms.
Treatment adherence is a serious concern, and relapse of symptoms is prevalent. Only roughly 60% of patients reach remission in 6 months.
Chronic illnesses, high interpersonal sensitivity, marital status, belonging to low socioeconomic status, and living alone are all risk factors for poor outcomes. Such individuals are at risk for suicide and premature unfavorable cardiac events.
https://www.ncbi.nlm.nih.gov/books/NBK430973/

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